Medical Presentation on autism for a class

I recently did a presentation on autism for a class I had.
Here are some interesting articles I found on it:
http://brain.oxfordjournals.org/cgi/content/full/125/8/1839" [Broken]
About the fusiform face area in autism.
http://brain.oxfordjournals.org/cgi/content/full/124/10/2059" [Broken]
Possible new treatments could be developed.
http://www.news.wisc.edu/10772.html" [Broken]
An autistic on being autistichttp://www.geocities.com/growingjoel/righttoexist.html"
There are currently a lot of techiniques out there that help autistics function better, but it would be interesting if current research yields a way for autistics to develop their fusiform face area because it might lessen some of the symptoms of the disorder. Do you guys think that there is any promise in this area?

Anatomical abnormalities, in contrast, were present only in the amygdala in autistic patients, whose mean volume was significantly reduced as compared with normals. Reaction time and accuracy measures were not different between groups. Thus, while autistic subjects could perform the face perception task, none of the regions supporting face processing in normals were found to be significantly active in the autistic subjects. Instead, in every autistic patient, faces maximally activated aberrant and individual-specific neural sites (e.g. frontal cortex, primary visual cortex, etc.), which was in contrast to the 100% consistency of maximal activation within the traditional fusiform face area (FFA) for every normal subject. It appears that, as compared with normal individuals, autistic individuals `see' faces utilizing different neural systems, with each patient doing so via a unique neural circuitry.

This is the first time I've seen anyone find the amygdala volume problem in autistic people, and the finding that each seems to develop their own idiosynchratic circuits for processing faces whereas "normals" all seem to use the same one, is a remarkable find.

Notably, the UW-Madison study overturns the existing notion that autistic children struggle to process faces because of a malfunction in the fusiform area. Rather, in autistic children the fusiform "is fundamentally normal" and shows only stunted activity because over-aroused amygdalas make autistic children want to look away, says senior author Richard Davidson, a UW-Madison psychiatry and psychology professor who has earned international recognition for his work on the neural underpinnings of emotion.

"Imagine walking through the world and interpreting every face that looks at you as a threat, even the face of your own mother," Davidson adds. Scientists have in the past speculated that the amygdala - which has been implicated in certain anxiety and mood disorders - plays a role in autism, but the study directly supports that idea for the first time.

An increasingly publicized developmental disability, autism greatly weakens the capacity to socialize and communicate normally. The tendency to avoid eye contact is one of the most pervasive traits among autistic children, says Dalton. The characteristic is a problem because eyes, in particular, are a crucial source of "subtle cues that are critical for normal social and emotional development," Dalton says.

Dalton's work comprised two studies. In the first, researchers placed autistic children inside an MRI scanner and showed them pictures of faces with both emotional and neutral expressions. The children had to press one of two buttons to indicate whether a face showed a blank or expressive face. Throughout the process, the researchers used precise eye-tracking technology to measure exactly which parts of the face study participants were looking at and for how long. Normally developing children far outpaced the autistic study participants in identifying expressions correctly.

During the second study, the researchers again placed subjects in MRI machines and showed them photographs of both familiar and unfamiliar faces. They monitored eye movements and brain activity, and once again, autistic subjects performed considerably more poorly than normally developing participants.

In the future, the findings could help scientists "train autistic children to look at a person's eye region in a more strategic way, like when the person may not be looking directly at them," says Davidson. Researchers eventually could assess whether such approaches improve the ability to make eye contact and whether they might even induce positive developmental changes in the brain.

Because autism is more inheritable than any other psychiatric condition, researchers also could start to explore the genetic mechanisms underlying hyperactive amygdalas -- "a completely uncharted research territory," says Davidson. And if the autistic amygdala is found to be overactive from infancy, the knowledge could help doctors implement intervention approaches right from an early age.

Above is from the wisconsin link.
****
I didn't know they had overturned the study findings that found that autistics have an abnormal fusiform face area until recently...
hopefully new therapies can be developed that can help with the overactive amygdala...

I took a look at the abstract at one link and was impressed by this:
This is the first time I've seen anyone find the amygdala volume problem in autistic people, and the finding that each seems to develop their own idiosynchratic circuits for processing faces whereas "normals" all seem to use the same one, is a remarkable find.

The possiblility the one could also "re-train" the autistic brain to interpret facial communcation and thus potentially ameliorate some of the problems associated with autism is also very fascinating. I remember hearing about early intervention in children with autism and how very intense socialization and training can lessen the impact of the disease. It reminds me of behavioral enrichment studies in animals and how this can sometimes counteract the effects of exposure to developmental toxicants.

The thing that really strikes me about autism is that it is marked by a wide constellation of cognitive and behavioral deficits which can vary greatly among individuals who have been diagnosed as autistic. It isn't likely that any one deficit will explain most of the variance, and it may also be that conditions that have all been labelled under the single term 'autism' on behavioral grounds may in fact reflect a number of largely distinct neuronal/cognitive deficits.

With regards to facial/emotion processing, for instance, in addition to the attention deficits mentioned here that may be due to heightened amygdala activity, it seems autistics may also have deficits in the functioning of their mirror neurons and as a result may have difficulty empathizing with the emotions of others (see here). So with regards to facial/emotion processing, there seems to be a spectrum of deficits. It would be interesting if further research could elucidate to what extent these deficits are independent vs. to what extent they interact and/or are caused by eachother.

I also find strange the discoveries that a) autistics may have overactive amydalas, and b) autistics may have anatomically smaller amygdalas. Perhaps they are missing some inhibitory neurons, which contributes to the overactivation? Perhaps chronic overactivation of the amygdala can cause amygdalar atrophy?

Perhaps chronic overactivation of the amygdala can cause amygdalar atrophy?

This makes me wonder if the "overactivation" isn't outright seizure activity. Fear sezures are about the most common simple partials after deja vu's. The amygdala/hippocampus combination is probably the most seizure prone of the whole brain. If the sight of two eyes looking at you automatically triggers a fear seizure, it would be no wonder they avoid it. Sending the image out to odd parts of the brain to be processed may be a way to avoid forming a mental image too close to the reality, which is just too frightening. A possible explanation for why a perfectly good fusiform gyrus goes unused.

Anyway, I know that alot of people with temporal lobe epilepsy show sclerotic hippocampi and this is assumed to be their seizure focus. The sclerosis doesn't preclude or prevent, but actually seems to cause, the "overactiviation" that a seizure represents. However, I'm not sure if they think repeated seizure activity causes the sclerosis or if they have other suspects.

It isn't likely that any one deficit will explain most of the variance, and it may also be that conditions that have all been labelled under the single term 'autism' on behavioral grounds may in fact reflect a number of largely distinct neuronal/cognitive deficits.

This is important to sort out. It might be a better idea to identify individuals with "Undersized Amydala Syndrome" and deal with that as such rather than get confused by everything that's fallen under an umbrella term and start wondering if this one is really Autism and that one not. It used to be asserted Autism was caused by an undersized cerebellum and many brain scans were presented demonstrating this. That particular problem should be examined in and of itself as "Undersized Cerebellum Syndrome" despite whatever symptoms it shares with "Undersized Amydala Syndrome" or whatever other known organic problems tend to have similar behavioral manifestations.

The thing that really strikes me about autism is that it is marked by a wide constellation of cognitive and behavioral deficits which can vary greatly among individuals who have been diagnosed as autistic. It isn't likely that any one deficit will explain most of the variance, and it may also be that conditions that have all been labelled under the single term 'autism' on behavioral grounds may in fact reflect a number of largely distinct neuronal/cognitive deficits.

Exactly...which is why I've often seen these cases collectivley referred to as "autism spectrum disorders".

hypnagogue said:

I also find strange the discoveries that a) autistics may have overactive amydalas, and b) autistics may have anatomically smaller amygdalas. Perhaps they are missing some inhibitory neurons, which contributes to the overactivation? Perhaps chronic overactivation of the amygdala can cause amygdalar atrophy?

Maybe the overactivation is an overcompensation due to the decreased size and potentially decreased output of this region? One can envision numerous feedback mechanisms that would be altered when practically any brain region is negatively impacted during development. Perhaps a cascade of events such as these leads to the disorder, the question is what is the first domino to fall?

To add an element in the discution: we have been talking about phisyological aspects in autism, but, there are also some interstig psycological issues too. For example, in "psycology of names" thay dicoverd that if a couple has a son that dies very young (like before 2 years) and than concive a second child and name him exactly as his death brother, there is a really high risk (70% or so) that this child develops autism. From Lacans point of view, the hidden message the kid recives behind his parents hugs and kisses is that he is actually death, so he learns to act that way. Independent of the interpretation, there is and undeniable correation in this.

Staff: Mentor

mandril said:

To add an element in the discution: we have been talking about phisyological aspects in autism, but, there are also some interstig psycological issues too. For example, in "psycology of names" thay dicoverd that if a couple has a son that dies very young (like before 2 years) and than concive a second child and name him exactly as his death brother, there is a really high risk (70% or so) that this child develops autism. From Lacans point of view, the hidden message the kid recives behind his parents hugs and kisses is that he is actually death, so he learns to act that way. Independent of the interpretation, there is and undeniable correation in this.

I have never heard of such a study, please post a link to it. My father was named after his dead older brother, and had no ill effects. I'd be curious to see how this study was conducted.